Showing papers by "Thomas J. Montville published in 1995"
TL;DR: It is determined that increasing protein or phospholipid concentrations decrease nisin 's effectiveness against Clostridium botulinum growth from spore inocula, and Nisin is also less effective at abuse compared to refrigerated temperatures.
90 citations
TL;DR: The results suggest that loss of ATP is due to attempts by the cell to maintain proton-motive force rather than the inability of thecell to produce ATP due to the loss of Pi.
Abstract: The bacteriocin pediocin PA-1 (80 AU ml -1 ), which is produced by Pediococcus acidilactici PAC 1.0, reduced Listeria monocytogenes Scott A viability by 4.6 log. Concomitant with the cell death, pediocin PA-1 induced irreversible K + and Pi efflux and ATP depletion in concentration-dependent and time-dependent fashions. The maximum amount of intracellular K + and Pi loss was 520 and 44.6 nmol mg -1 CDW, respectively. Intracellular ATP levels decreased from 2.8 to 0.029 nmol mg -1 CDW, corresponding to 98.9% depletion. Less than 0.1% ATP efflux was found with pediocin concentrations up to 200 AU ml -1 . Approximately 10, 40 and 60 min were required for maximum K + efflux, ATP depletion and Pi efflux, respectively. Moreover, pediocin PA-1 depleted 90% of cytoplasmic ATP when only 25% Pi efflux took place. These results suggest that loss of ATP is due to attempts by the cell to maintain proton-motive force rather than the inability of the cell to produce ATP due to the loss of Pi. Dithiothreitol-treated PA-1 no longer inhibited the growth of L. monocytogenes cells, and caused neither concentration-dependent ion efflux nor ATP depletion.
79 citations
TL;DR: The nature of and reasons for the varied regulatory and industrial responses aimed at preventing listeriosis and L. monocytogenes contamination in ready-to-eat foods are examined, and a paradigm for dealing with novel foodborne pathogens in the future is proposed.
Abstract: The emergence of Listeria monocytogenes as a foodborne pathogen in the USA during the 1980s prompted rapid, but often overlapping and conflicting, responses by the US Food and Drug Administration, the US Department of Agriculture and the food industry. Nonetheless, because of these responses, there have been no outbreaks of foodborne listeriosis reported in the USA during the past nine years. This article briefly discusses the history and etiology of listeriosis, and examines the nature of and reasons for the varied regulatory and industrial responses aimed at preventing listeriosis and L. monocytogenes contamination in ready-to-eat foods. Based on the experience gained from the response to L. monocytogenes , a paradigm for dealing with novel foodborne pathogens in the future is proposed.
26 citations